Chest Pain

Jonathon D. Pa lmer, MD

Key Points

• Chest pain is a very common complaint in emergency

department patients.

• A rapid electrocardiogram and chest x-ray will help distinguish between multiple emergent causes of chest pain.

INTRODUCTION

Chest pain is one of the most common presenting complaints in the emergency department (ED). As several fatal

�

onditions present with chest pain, it is imperative to rapIdly and thoroughly evaluate these patients to distinguish

between emergent and nonemergent causes. Approach

chest pain with a broad differential diagnosis and utilize

your history, physical exam, and ancillary testing to narrow

down the etiology.

The pathophysiology of chest pain will vary tremendously depending on the specific etiology. Regardless of

the source, pain sensation ultimately occurs owing to

stimulation of either visceral or somatic nerve fibers.

Somatic nerve fibers innervate the skin and parietal pleura.

Patients will typically complain of a pain that is sharp in

nature and easily localized. Potential etiologies include

pulmonary embolism, pneumothorax, musculoskeletal

injury, herpes zoster infection, pneumonia, and pleurisy.

Conversely, visceral nerve pain is often vague in quality,

poorly localized, and will frequently radiate to nearby

structures. Patients may deny the actual sensation of "pain"

and rather describe their condition as a heaviness, pressure, or simple discomfort. Potential etiologies include

acute coronary syndrome (ACS), aortic dissection, gastro ­

esophageal reflux, and pericarditis.

46

• The exclusion of life-threatening sources of chest pain

should be the emergency physicia n's chief diagnostic

concern.

CLINICAL PRESENTATION

� History

A detailed history is essential when evaluating patients

with chest pain, as no single element in isolation is sensi ­

tive or specific enough to determine either the etiology or

the severity of the complaint. Ascertain the character of the

pain to help determine a somatic or visceral source. For

example, a sharp and stabbing pain is less likely in patients

with ACS, but rather common in patients with pulmonary

embolism. Identify the exact location of the pain and

whether there is any associated radiation. Prototypical

ischemic chest pain presents either just beneath the sternum or on the left side and radiates to either the left arm

or jaw, whereas a mid-thoracic "tearing type" pain radiating straight through to the back is classically associated

with aortic dissection. Determine the severity and duration

of the pain. A mild, sharp pain lasting only seconds in

duration is rarely associated with a serious pathology,

whereas pain lasting greater than 10 minutes may suggest a

more serious etiology. Recurrent pain that lasts for many

hours or days per episode is unlikely to be cardiac.

In patients with a known history of heart disease, ascertain whether or not their symptoms mirror prior presenta ­

tions. Patients with pain that is either similar to or more

severe than a previous myocardial infarction (MI) have a

markedly increased likelihood of ACS. Identify exacerbating or relieving factors, as this can quickly impact manage ­

ment. Patients with potential cardiac presentations

frequently complain of pain that is worse with exertion

and improved with rest. Pain that is worse with cough or

deep inspiration (pleuritic pain) is typically associated

with either pleurisy, a musculoskeletal etiology, or pulmo ­

nary embolism. Epigastric pain that is worse with meals

usually signifies a gastrointestinal etiology. Pain that is

aggravated by emotional stress may point to an underlying

psychiatric etiology. Finally, inquire about any associated

symptoms. For example, nausea and diaphoresis have been

associated with a higher likelihood for ACS.

Unfortunately, the long-term risk factors for underlying

heart disease (high cholesterol, smoking, hypertension, diabetes, family history) have not been shown to help in the

differentiation of acute chest pain patients in the ED. Nonetheless, this history should be taken. A history of an underlying hypercoagulable state ( eg, pregnancy, malignancy) should

alert you to a possible pulmonary embolism (PE), whereas a

history of an underlying connective tissue disorder ( eg,

Marfan syndrome) should prompt an evaluation for aortic

dissection. Ask about any illicit drug habits, as cocaine use

has been associated with accelerated atherosclerosis, acute

MI, and aortic dissection.

� Physical Examination

Note the general appearance of the patient. Those with

ACS or other serious etiologies may be clutching their

chest and frequently appear anxious, pale, and diaphoretic.

This "sick vs not sick" mentality will guide the rapidity of

your examination. As with all emergency patients, assess

the vital signs and ensure adequate airway, breathing, and

circulation (ABCs). Note abnormal vital signs to help

guide your differential diagnosis. A detailed examination

of the heart, lungs, abdomen, extremities, and neurologic

systems will ensure that no emergent causes of chest pain

are overlooked. Listed next are some emergent presenta ­

tions matched with potential physical exam findings.

ACS. Vital signs will vary widely depending on the re ­

gion of ischemia or infarction. For example, an inferior

wall MI may present with bradycardia and hypotension

owing to increased vagal tone. Murmurs and abnormal

heart sounds such as an S3 or S4 may be present. I nspiratory crackles on 1 ung exam are consistent with secondary

pulmonary edema.

Tension pneumothorax. Look for the classic signs of

decreased breath sounds, tracheal deviation, and res piratory distress. Consider spontaneous pneumothorax in

young, thin patients with an acute onset of chest pain

and shortness of breath.

Pericardia! tamponade. Although usually limited to

patients in extremis, patients may exhibit the classic

signs of Beck's triad (hypotension, diminished heart

CHEST PAIN

sounds, and jugular venous distension). Pulsus paradoxus > 10 mmHg has shown a high sensitivity but low

specificity for tamponade, as any condition causing increased intrathoracic pressure may demonstrate this.

Pulmonary embolism. Dyspnea is the most common

complaint of patients with PE. They may also describe a

pleuritic-type chest pain, especially those with segmental

PEs that cause secondary infarction of the parietal pleura.

Patients with significantly large (massive or submassive)

PE are generally ill-appearing and hemodynamically unstable owing to the sudden severe increase in pulmonary

vascular resistance. A detailed examination of the heart

and lungs may reveal rales, gallops, or a prominent P2.

Lower extremity exam may reveal unilateral swelling consistent with a deep venous thrombosis.

Aortic dissection. The pain is often most severe at onset

and typically extends above and below the diaphragm.

These patients are often hypertensive and may have a

pulse deficit in either the radial and/or femoral arteries.

A marked discrepancy in blood pressure compared between each arm (>20 mmHg) is highly suggestive.

DIAGNOSTIC STUDIES

Perform an electrocardiogram (ECG) within 10 minutes of

presentation for all patients who complain of chest pain or

have signs and symptoms concerning for ACS. Obtain cardiac

markers including a troponin assay ± CK-MB analysis in all

patients with suspected ACS. D-dimer can aid the evaluation

of low-risk patients in whom PE is a diagnostic possibility.

CXR should be ordered on most patients in the ED with

chest pain. Posteroanterior and lateral views are ideal, but a

portable anteroposterior view is sufficient for patients who

require continuous cardiac monitoring. Acute aortic dissection may present with a widened mediastinum or abnormal

aortic contour. Pneumothoraces and subcutaneous air are

readily identified. Pneumomediastinum ± a left-sided pleural

effusion (owing to the relative thinness of the left esophageal

wall) is seen with esophageal rupture (Boerhaave syndrome).

Newer generation CT angiography is the modality of

choice to diagnose pulmonary embolism and aortic dissection and may have an evolving role in the evaluation of

patients with potential coronary artery disease.

Transthoracic echo is often readily available and clinically useful to evaluate for possible pericardia! effusions

and tamponade physiology, ventricular hypokinesis in

patients with ACS, and right ventricular strain in patients

with massive PE. A bedside transesophageal echo is very

sensitive for diagnosing acute aortic dissection in patients

who are not candidates for CT angiography.

MEDICAL DECISION MAKING

A detailed history and physical exam in combination with

an ECG and/or chest radiograph may provide sufficient

evidence to exclude a myriad of emergent conditions.

CHAPTER 13

Patient presenting with

chest pain

Rapidly address ABC's, IV access,

supplemental 02 and cardiac mon itor

Immediate ECG and CXR

Absent breath

sounds with

shock

Pain radiates to

the back with wide

mediastinum on CXR

ECG with ischemia

or positive troponin

Pleuritic CP,

hypoxia, + CT

angiogram

History of vomiti ng,

mediastinal air on

CXR

Hypotension,

JVD, muffled

heart tones

.&. Figure 13-1. Chest pain diagnostic algorithm. BMP, basic metabolic panel; BP, blood pressure; CBC, complete blood

count; CP, chest pain; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiogram; JVD, jugular venous distention.

When this is not adequate, a thoughtful use of laboratory

studies combined with the pretest probability of disease

will guide decision making (Figure 13-1).

TREATMENT

� Acute Coronary Syndrome

Provide supplemental 0 2, administer a loading dose aspirin

(162-365 mg), and begin sublingual nitroglycerin (0.4 mg

every 5 minutes) on all ACS patients without known contraindications (eg, allergy, hypotension). Further antithrombotic

(eg, clopidogrel) and anticoagulation (eg, low-molecularweight heparin) therapy will differ by institution and cardiologist. Of note, the preceding interventions are often only

temporizing measures, as early revascularization is definitive,

especially in those patients presenting with an ST -elevation MI.

� Aortic Dissection

Patients with an aortic dissection require an immediate

and aggressive reduction in both heart rate and blood pressure. The goal of treatment is to maintain a heart rate

<60 bpm and systolic blood pressure < 100 mmHg. There

are multiple medication options for this purpose, and

often concurrent infusions are required to meet the pre ­

ceding targets. When utilizing dual therapy, it is of utmost

importance to control the heart rate before dropping the

blood pressure to avoid a "reflex tachycardia" and conse ­

quent expansion of the underlying dissection.

� Pulmonary Embolism

Treatment will vary based on the hemodynamic impact of

the embolism. Anticoagulate stable patients with either

low-molecular-weight or unfractionated heparin. Hemo ­

dynamic instability may necessitate the use of thrombolytic

therapy.

..... Boerhaave Syndrome

Esophageal rupture is uncommon and classically presents

with the sudden onset of chest pain after vomiting. Initiate

broad-spectrum antibiotic coverage while arranging for

definitive surgical repair.

..... Pneumothorax

Place all patients with a pneumothorax on s upplemental 02

via a nonrebreather mask. Those with a tension pneumothorax require immediate needle decompression followed

by chest tube thoracostomy. Simple pneumothoraces can be

treated with tube thoracostomy or simple observation.

..... Pericardia! Tamponade

The recognition of tamponade is much easier in the age of

bedside ultrasonography. Perform immediate pericardio ­

centesis in unstable patients while arranging for an operative pericardia! window via cardiothoracic surgery.

DISPOSITION

...,_ Admission

Admit all patients with concerning presentations to a

monitored bed. The following chapters discuss the

CHEST PAIN

disposition of patients with specific conditions m

greater detail.

..... Discharge

Many patients with chest pain can be discharged with close

primary care follow-up and a list of strict indications for

reevaluation. Take care to exclude emergent causes and

discharge only those cases with a clear nonemergent etiology (eg, chest wall pain, zoster, dyspepsia). If clinical doubt

exists, it is certainly prudent to err on the side of caution

and admit for inpatient observation.

SUGGESTED READING

Anderson JL, Adams CD, Antman EM, et al. ACC/ AHA 2007

Guidelines for the management of patients with unstable

angina/non ST-elevation MI: A report of the ACC/AHA

task force of practice guidelines. Circulation. 2007;116:

el48.

Fesmire FM, Brown MD, Espinosa JA, et a!. Critical issues in the

evaluation and management of adult patients presenting to

the emergency department with suspected pulmonary embolism. Ann Emerg Med. 20 1 1;57:628-652.

Green GB, Hill PM. Chest pain: Cardiac or not. I n: Tintinalli

JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler

GD. Tintinalli's Emergency Medicine: A Comprehensive

Study Guide. 7th ed. New York, NY: McGraw-Hill, 20 1 1,

pp. 36 1-367 .

Swap CJ, Nagumey JT. Value and limitations of chest pain his ­

tory in the evaluation of patients with acute coronary syn ­

dromes. JAMA. 2005;294:2623-2639.